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Glucocorticoid receptors (GR) are ubiquitously expressed in metazoans. Different and contrasting phenotypes have been reported upon their activation. This study investigated the behavioral phenotypes characteristic of GR stimulation in male Wistar rats. Rats in each of the four groups of rats received one of the following treatments: distilled water (control) or one of three doses of dexamethasone (treatment) injected intraperitoneally for 7 days. The Rats were afterwards subjected to the Y maze, the elevated plus maze (EPM), the Morris water maze (MWM), and the novel object recognition (NOR) test. At the end of the study, the animals were anesthetized and neural activity from the prefrontal cortex recorded. Blood was collected via cardiac puncture to evaluate the levels of plasma insulin and glucose, and the prefrontal cortexes excised to determine the levels of insulin, markers of oxidative stress, and calcium in the homogenate. This study showed that treatment with dexamethasone significantly reduced the total and percentage alternation in the Y maze, but had no significant effect on object recognition in the NOR test, long-term and short-term spatial memory in the MWM, or anxiety-like behavior in the EPM. Plasma and brain insulin and calcium levels were elevated moderately following treatment with the lowest dose of dexamethasone. All doses of dexamethasone decreased brain superoxide dismutase and increased lactate dehydrogenase levels. No significant change in neural activity was observed. This study shows that activation of glucocorticoid receptors differentially affects different behavioral paradigms and provides evidence for a role for glucocorticoids in mediating insulin function in the brain., (Copyright © 2017 Elsevier B.V. All rights reserved.)

Although oxidative stress is characteristic of global vascular occlusion and cyanide toxicity, the pattern of cerebral metabolism reconditioning and rate of progression or reversal of neural tissue damage differ for both forms of ischemia. Thus, it is important to compare cognitive and motor functions in both models of ischemia involving cyanide treatment (CN) and vascular occlusion (VO). Adult Wistar rats (N=30) were divided into three groups; VO (n=12), CN (n=12) and Control-CO (n=6). The CN was treated with 30mg/Kg of potassium cyanide (KCN); VO was subjected to global vascular occlusion-both for duration of 10 days. The control (CO) was fed on normal rat chow and water for the same duration. At day 10, the test and control groups (CN, VO and CO) were subjected to motor function tests (Table edge tests and Open Field Test) and memory function tests (Y-Maze and Novel object recognition) while the withdrawal groups CN-I and VO-I were subjected to the same set of tests at day 20 (the withdrawal phase). The results show that both cyanide toxicity and vascular occlusion caused a decline in motor and memory function when compared with the control. Also, the cyanide treatment produced a more rapid decline in these behavioral parameters when compared with the vascular occlusion during the treatment phase. After the withdrawal phase, cyanide treatment (CN-I) showed either an improvement or restoration of motor and memory function when compared to the CN and control. Withdrawal of vascular occlusion caused no improvement, and in some cases a decline in motor and memory function. In conclusion, cyanide toxicity caused a decline in motor and memory function after the treatment while vascular occlusion caused no significant decline in cognition and motor function at this time. After the withdrawal phase, the effect of cyanide toxicity was reduced and significant improvements were observed in the behavioral tests (motor and cognitive), while a decline in these functions were seen in the vascular occlusion group after this phase., (Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.)

Background: Vascular occlusion and cyanide neurotoxicity induces oxidative stress and degeneration in the brain. This oxidant induced stress changes the vascular dynamics of cerebral blood vessels, and participates in homeostatic response mechanisms which balance oxygen supply to hypoxic stress-sensitive neurons. The associated changes in vascular morphology include remodeling of the microvasculature and endothelial changes, alterations in regional circulation and variations in the blood brain barrier (BBB). This study compares alterations in physiology of the cerebral artery after a short-term oxidative stress induced by cyanide toxicity and vascular occlusion., Method: Adult Wistar rats (N=30) were divided into three groups; vascular occlusion (VO) (n=12), potassium cyanide administration (CN) (n=12) and Control-CO (n=6). The CN rates were treated with 30mg/kg of orally administered KCN while the VO was subjected to global vascular occlusion, both for a duration of 10 days, described as the treatment phase. Control animals were fed on normal rat chow and water for 10 days. At the end of the treatment phase, n=6 animals in each of the VO, CN and VO groups were anesthetized with sodium pentobarbital (50IP) and the CCA exposed, after which pin electrodes were implanted to record the spikes form the tunica media of the CCA. After day 10, treatment was discontinued for these animals, each remaining in the VO and CN groups (VO-I and CN-I) until day 20 (withdrawal phase) following which the spikes were recorded using the procedure described above., Results/discussion: Vascular occlusion and cyanide toxicity increased vascular resistance in the MCA (reduced lumen thickness ratio) and increased the diameter of the CCA after the treatment phase of 10 days. After 10 days of withdrawal, the VO group showed a reduction in resistance and an increase in the lumen width/wall thickness ratio (LWR) while the CN group showed increased resistance and a reduction in LWR., Conclusion: Cyanide toxicity increased vascular resistance by inducing degenerative changes in the wall of the artery while vascular occlusion increased resistance through mechanical stress and increased thickness of arterial wall. After the withdrawal phase, vascular resistance diminished in the VO to a significantly greater extent than the CN., (Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.)